Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA.
Int J Rheum Dis. 2014 May;17(4):359-68. doi: 10.1111/1756-185X.12293. Epub 2014 Jan 27.
Rheumatoid arthritis (RA) can be the source of significant pain and functional limitation. The past 20 years have seen a transition in treatment goals away from mere pain management toward disease modification through the suppression of autoimmunity. Disease-modifying anti-rheumatic drugs, such as methotrexate and biologic agents, impair disease progression and joint destruction. However, despite these achievements, a substantial subset of RA patients does not respond to or cannot tolerate current treatments for RA. Scientific insight into the cellular pathways of inflammation has revealed new therapeutic targets for the treatment of autoimmune diseases like RA. Attention has focused on pathways mediated by Janus kinase (JAK), mitogen-activated protein kinase (MAPK), and spleen tyrosine kinase (Syk). This review article summarizes the evidence supporting the use of various kinase inhibitors, including the newly approved JAK inhibitor tofacitinib, in the treatment of RA.
类风湿关节炎（RA）可导致严重疼痛和功能受限。过去 20 年中，治疗目标已从单纯的疼痛管理转向通过抑制自身免疫来实现疾病缓解。甲氨蝶呤和生物制剂等疾病修饰抗风湿药物可延缓疾病进展和关节破坏。然而，尽管取得了这些成就，仍有相当一部分 RA 患者对当前的 RA 治疗无反应或无法耐受。对炎症细胞通路的科学认识揭示了治疗 RA 等自身免疫性疾病的新治疗靶点。人们关注的焦点是由 Janus 激酶（JAK）、丝裂原活化蛋白激酶（MAPK）和脾酪氨酸激酶（Syk）介导的通路。本文综述了支持使用各种激酶抑制剂（包括新批准的 JAK 抑制剂托法替布）治疗 RA 的证据。
